The toxicity of symptomology of chlordimeform and several metabolites following various modes of treatment of rats were examined. The symptoms manifested by poisoned rats indicated nervous system involvement. Two metabolites, demethylchlordimeform and didemethylchlordimeform, were more toxic and faster acting than the parent compound, suggesting that in rats sequential oxidative N-demethylation of chlordimeform was an activation reaction. Monoamine oxidase (MAO) was inhibited in rats treated with chlordimeform and several related compounds including the formanilide 4-chloro-o-formotoluidide. However, there was no apparent relationship between toxicity and MAO inhibition. Forty-two formanilides were examined for their potency as in vitro inhibitors of rat brain MAO. Structure-activity relationship data with serotonin, dopamine, and tryptamine as substrates indicated that for maximum MAO inhibitory potency formanilides should be substituted in ring position 2 and 5, 2 and 4, or 4 and 5. With beta-phenylethylamine as substrate maximum inhibitory potency was associated with chlorine in ring position 3 and chlorine or methyl in ring position 2 or 4. Metabolism studies of radiolabeled formetanate, oxamyl, and methomyl in twospotted spider mites indicated that the acaricides were rapidly absorbed and converted to other products, some of which were identified. The metabolic paths for these compounds in mites generally were similar to those reported previously for mammals, however, quantitative differences were evident.